The effects of acute ethanol administration on an in vitro protein synthesizing system from rat brain

1972 ◽  
Vol 44 (2) ◽  
pp. 698-700 ◽  
Author(s):  
Carlos Lamar
1976 ◽  
Vol 160 (2) ◽  
pp. 315-324 ◽  
Author(s):  
A A Badawy ◽  
M Evans

1. Acute administration of ethanol exerts a biphasic effect on the concentrations of rat brain tryptophan, 5-hydroxytryptamine and 5-hydroxyindol-3-ylacetic acid. Both effects are associated with corresponding changes in the availability of circulating free tryptophan. 2. The initial increases in the above concentrations are prevented by ergotamine, are unaltered by allopurinol and are potentiated by theophylline, whereas the later decreases are prevented by both ergotamine and allopurinol. 3. It is suggested that the initial enhancement by ethanol of brain tryptophan metabolism is caused by catecholamine-mediated lipolysis followed by displacement of protein-bound serum tryptophan, whereas the activation of liver tryptophaan pyrrolase, which is produced by the same mechanism, leads to the later decreases in the brain concentrations of tryptophan and its metabolites. 4. The initial effects of ethanol can be reproduced by an equicaloric dose of sucrose, and a comparison of the two treatments alone could therefore be misleading. 5. The effects of ethanol on liver and brain tryptophan metabolism have also been examined in mice, and a comparison of the results with those previously reported suggests that the ethanol effects are strain-dependent.


1981 ◽  
Vol 241 (2) ◽  
pp. G176-G181
Author(s):  
R. S. Green ◽  
R. G. MacDermid ◽  
R. L. Scheig ◽  
J. J. Hajjar

The acute effect of ethanol on amino acid absorption across the in vivo rat intestine was studied using single-pass continuous perfusion and recirculation techniques. The single-pass steady-state perfusion was used to examine the effect on the entire small intestine and recirculation perfusion to examine the effect on short intestinal segments and to limit ethanol absorption. Unlike the in vitro findings of other investigators, ethanol does not cause inhibition of net amino acid absorption in vivo unless the alcohol is perfused in 2 M or higher concentrations. The inhibition that is observed at these concentrations is very likely due to severe injury and shedding of intestinal cells as evidenced by an increased recovery of DNA in the perfusates. The findings suggest that acute ethanol administration, in concentrations that are comparable to those found in the upper intestines of humans after the ingestion of moderate doses of alcohol, does not have a prominent effect on amino acid absorption across the in situ rat intestine. Under these conditions, the ethanol inhibition of active absorption is masked by enhanced diffusion of the amino acids across the intestine.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Huimin Liu ◽  
Wenbin Zheng ◽  
Gen Yan ◽  
Baoguo Liu ◽  
Lingmei Kong ◽  
...  

The aim of this study is to describe the acute effects of EtOH on brain edema and cerebral metabolites, using diffusion weight imaging (DWI) and proton magnetic resonance spectroscopy (1H-MRS) at a 7.0T MR and to define changes in apparent diffusion coefficient (ADC) values and the concentration of metabolites in the rat brain after acute EtOH intoxication. ADC values in each ROI decreased significantly at 1 h and 3 h after ethanol administration. ADC values in frontal lobe were decreased significantly compared with other regions at 3 h. For EtOH/Cr+PCr and cerebral metabolites (Cho, Tau, and Glu) differing over time, no significant differences for Ins, NAA, and Cr were observed in frontal lobes. Regression analysis revealed a significant association between TSEtOH/Cr+PCrand TSCho, TSTau, TSGlu, and TSADC. The changes of ADC values in different brain regions reflect the process of the cytotoxic edema in vivo. The characterization of frontal lobes metabolites changes and the correlations between TSEtOH/Cr+PCrand TSCho, TSTau, and TSGluprovide a better understanding for the biological mechanisms in neurotoxic effects of EtOH on the brain. In addition, the correlations between TSEtOH/Cr+PCrand TSADCwill help us to understand development of the ethanol-induced brain cytotoxic edema.


2000 ◽  
Vol 37 (5-6) ◽  
pp. 483-496 ◽  
Author(s):  
P de Gortari ◽  
M Méndez ◽  
I Rodrı́guez-Keller ◽  
L Pérez-Martı́nez ◽  
P Joseph-Bravo

1971 ◽  
Vol 49 (5) ◽  
pp. 481-483 ◽  
Author(s):  
D. C. Villeneuve ◽  
W. E. J. Phillips

Both the oral and intraperitoneal administration of acute doses of ethanol resulted in decreased toxicity of parathion in the rat. The rate of in vitro parathion degradation by liver homogenates from rats administered ethanol by the oral route was lower than in the control rats. These results indicate that the altered toxicity is not due to enzyme induction.


1990 ◽  
Vol 11 (3) ◽  
pp. 209-216 ◽  
Author(s):  
Gail V.W. Johnson ◽  
Keith W. Cogdill ◽  
Richard S. Jope

1976 ◽  
Vol 27 (2) ◽  
pp. 471-475 ◽  
Author(s):  
Martin M. Widelitz ◽  
Marlene R. Coryell ◽  
Howard Widelitz ◽  
Narayan G. Avadhani

Neuropeptides ◽  
2010 ◽  
Vol 44 (5) ◽  
pp. 413-420 ◽  
Author(s):  
M. Méndez ◽  
I.G. Barbosa-Luna ◽  
J.M. Pérez-Luna ◽  
A. Cupo ◽  
J. Oikawa

1985 ◽  
Vol 249 (2) ◽  
pp. G177-G183 ◽  
Author(s):  
J. J. Hajjar ◽  
E. R. Baker ◽  
D. M. Renison ◽  
P. W. Gardner ◽  
R. Zirin ◽  
...  

The effect of ethanol on choline transport across the rat jejunum was studied by intraluminal perfusion in vivo and by influx measurement across the brush-border membrane in vitro. Acute ethanol administration (4 g/kg) through a gastric tube caused an increase in net choline absorption within 1 h. The increase was prevented by pretreatment with pyrazole, an inhibitor of ethanol metabolism. Chronic ethanol administration also caused an increase in choline absorption, the effect being unrelated to the nutritional changes that occur with ethanol ingestion. In contrast, direct instillation of 0.65 M ethanol through the perfusate caused no changes in choline absorption, and the perfusion of a 1.14 M solution even decreased absorption. The in vitro influx of choline across the mucosal membrane of the isolated rat jejunum was also enhanced by pretreatment with ethanol given by gavage 1 h prior to experimentation. Similarly, the ethanol-related increase in the influx rate was inhibited by pyrazole but was unaffected by acetaldehyde or acetate. Like ethanol, pretreatment of rats with methanol stimulated the choline influx rate. The results suggest that ethanol metabolism, rather than the direct effect of ethanol by itself, stimulates the absorption and influx of choline into the rat jejunum. The effect is not produced by the primary metabolites of ethanol, acetaldehyde, or acetate but is very likely related to stimulation by other products of ethanol metabolism.


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